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In this study, researchers observed that a noncanonical mechanism involving the γ-secretase-dependent, RBPj-independent Notch intracellular domain improves survival in Msx2-Cre mice by delaying hair follicle destruction and reducing disease severity.

In this study, two unique mutations in the RBPJ gene were identified and linked to Adams-Oliver syndrome, confirming impaired DNA binding of mutated RBPJ as a factor in this rare genetic disorder.

This study found that the acceleration of endothelial to mesenchymal transition due to loss of Notch signaling led to delayed wound healing and increased scarring in skin wounds.

In this study, the researchers reported that Notch/CSL signaling is crucial for hair follicle differentiation, with Wnt5a signaling and FoxN1 acting as mediators in mice.

This article reviews mammalian skin epidermis as a model for studying stem cell regulation, noting the utility of in vitro and ex vivo platforms, but it reports no new empirical findings.